Control of Biosynthesis of Host Macromolecules in Cells Infected with Adenoviruses

Ginsberg, Harold S.; Bello, Leonard J.; Levine, Arnold J.

doi:10.1016/b978-0-12-395717-7.50036-5

Cited by 73 publications

(43 citation statements)

References 39 publications

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“…Several authors have shown that when the rate of viral DNA replication is at its maximum the synthesis of host-cell DNA is suppressed (Ginsberg et al, 1967;Pearson and Hanawalt, 1971). On the other hand a stimulation of cellular DNA synthesis under these conditions is reported by Takahashi et al (1969).…”

Section: Discussionmentioning

confidence: 99%

Localization of adenovirus DNA replication in KB cells

1975

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The localization of adenovirus type 5 DNA replication has been investigated by both fractionation of isolated nuclei and electron-microscope autoradiography. Biol. 40,[65][66][67][68][69][70][71][72][73][74][75][76] reveals that pulse-labeled adenovirus type 5 DNA cosediments with the nuclear membrane. On the basis of this finding it can be supposed that the site of viral DNA replication is at the nuclear membrane. However, electron-microscope autoradiography of infected cells shows that the pulse-labeled viral DNA is not located at the nuclear membrane but randomly distributed over the nucleus. It is concluded that the replication of adenovirus type 5 DNA occurs throughout the cell nucleus; the association of replicating viral DNA with a nuclear membrane complex should be considered as an artifact.

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Section: Discussionmentioning

confidence: 99%

Localization of adenovirus DNA replication in KB cells

1975

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“…This 5' region is called the tripartite leader because it is coded by three noncontiguous viral DNA segments that are located between the major start site for late transcription and the late proteincoding regions (for a review, see reference 59). Concomitant with the induction of late transcription, host cell protein synthesis is repressed, and late viral mRNAs are preferentially translated (16,46). The function of the tripartite leader is not fully understood, but there are data which suggest that the leader is a signal that identifies late viral mRNAs for selective translation (4,30,57 indicated that a nearly complete tripartite leader is necessary for optimal levels of hybrid mRNA translation during the late phase of infection.…”

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confidence: 99%

Downstream sequences affect transcription initiation from the adenovirus major late promoter.

Mansour¹,

Grodzicker²,

Tjian³

1986

Mol. Cell. Biol.

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We analyzed a set of adenovirus-simian virus 40 (SV40) hybrids in which the SV40 T antigen coding sequences are inserted downstream from the adenovirus major late promoter within the first, second, and third segments of the tripartite leader. In infected cells, these viruses give rise to a matched set of hybrid SV40 mRNAs that differ only in the number of tripartite leader segments attached to the complete SV40 T antigen coding region. We found that the number of tripartite leader segments present at the 5' end of the hybrid SV40 mRNAs had little effect on the efficiency of T antigen translation. Surprisingly, insertion of SV40 sequences within the first leader segment, at +33 relative to the start of transcription, significantly reduced the frequency of transcription initiation from the major late promoter. The 3' boundary of this downstream transcriptional control element was mapped between +33 and + 190 by showing that insertion of SV40 sequences within the intron after the first leader segment at + 190 had very little effect on transcription initiation from the late promoter. A transient expression assay was used to show that the effect of downstream sequences on transcription initiation from the major late promoter is dependent on a trans-acting factor encoded or induced by adenovirus.In a permissive host, the human adenoviruses, which have a double-stranded DNA genome of 36,000 base pairs, undergo a regulated program of gene expression that is divided into early and late phases, demarcated by the initiation of viral DNA replication. During the late phase of infection, viral transcription initiates primarily from the major late promoter, giving rise to primary transcripts that are processed by differential splicing and polyadenylation into more than 30 mRNA species. Each of the late mRNAs carries at its 5' end a common 203-nucleotide untranslated sequence that is spliced to a protein-coding sequence. This 5' region is called the tripartite leader because it is coded by three noncontiguous viral DNA segments that are located between the major start site for late transcription and the late proteincoding regions (for a review, see reference 59). Concomitant with the induction of late transcription, host cell protein synthesis is repressed, and late viral mRNAs are preferentially translated (16,46). The function of the tripartite leader is not fully understood, but there are data which suggest that the leader is a signal that identifies late viral mRNAs for selective translation (4,30,57 indicated that a nearly complete tripartite leader is necessary for optimal levels of hybrid mRNA translation during the late phase of infection. However, it was not possible to use these recombinant viruses to assess systematically the contribution of cis control sequences to late promoter activity because the Ela enhancer is located upstream of the hybrid transcription unit and is likely to affect its activity. Moreover, the hybrid transcription units are missing the intron sequences between the leader segments, and thus pote...

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“…One aspect of the adenovirus-host cell interaction has, however, received much less attention: the extremely efficient usurpation of the cellular biosynthetic machinery, characteristic of the late phase of infection, is a well-established phenomenon, but one whose molecular basis has been little investigated. Inhibition of cellular DNA synthesis by adenoviruses begins with the initiation of viral DNA synthesis (and, by definition, the late phase) some 6 to 8 h after infection by type C adenovirus (adenovirus type 2 [Ad2] or AdS) and is essentially complete a few hours thereafter (9,25). Similarly, only adenoviral polypeptides are labeled once the late phase is established (1, 2, 28, 39).…”

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Effects of adenovirus infection on rRNA synthesis and maturation in HeLa cells.

Castiglia¹,

Flint²

1983

Mol. Cell. Biol.

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Virology 40:893-902, 1970). However, the effects on 28S cytoplasmic rRNA were observed considerably earlier in the infectious cycle than those on 18S rRNA. The inhibition of cellular protein synthesis and of the appearance in the cytoplasm of labeled cellular mRNA sequences (G. A. Beltz and S. J. Flint, J. Mol. Biol. 131:353-373, 1979) were also monitored in infected cultures. During the later periods of an infectious cycle, from 18 h after infection, nucleolar rRNA synthesis and processing and exit of 18S rRNA from the nucleus were inhibited, probably reflecting the failure of infected cells to synthesize normal quantities of ribosomal proteins. The earliest responses of cellular RNA metabolism to adenovirus infection were, however, the rapid and apparently coordinate reductions in the levels of newly synthesized 28S rRNA and cellular mRNA sequences entering the cytoplasm.

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Control of Biosynthesis of Host Macromolecules in Cells Infected with Adenoviruses

Cited by 73 publications

References 39 publications

Localization of adenovirus DNA replication in KB cells

Localization of adenovirus DNA replication in KB cells

Downstream sequences affect transcription initiation from the adenovirus major late promoter.

Effects of adenovirus infection on rRNA synthesis and maturation in HeLa cells.

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